Adjuvant arthritis is an experimental disease unique to rats that resembles the human spondyloarthropathies. The disease is induced in rats by a single inoculation of a lipid solvent containing a bacterial cell wall product. The disease can be produced in a normal rat by intravenous injection of lymphocytes from an arthritic rat. Substantial other evidence for a primary immunopathogenesis has accumulated from many studies. The current model of the immune system postulates a network of separate but interacting cells, each with a specific genetically defined function. Functional groups of cells have been shown to be identifiable by characteristic cell surface molecules. Recent advances have permitted the development of monoclonal antibodies that detect such surface markers on different functional groups of rat T lymphocytes. Methods are available for using these monoclonal antibodies to isolate large quantities of different groups of T cells that react with the different antibodies. I propose to use these methods to separate lymphocytes from rats with adjuvant arthritis, and, by transfer of cells to recipient rats, to discover which functional subpopulations of lymphocytes lead to the subsequent development of the arthritic disease. I shall also explore potential augmenting and suppressing interactions of these cells with other cell subpopulations. This animal disease is likely to serve as a useful model of the human reactive arthritic diseases, such as Reiter's syndrome, in which certain bacterial infections trigger subsequent arthritis. The association of these diseases with gene products of the HLA complex suggest that immunologic mechanisms may play a primary pathogenic role in these human diseases; recent studies support this hypothesis. Achieving the aim of this project-elucidation of the roles of specific subsets of lymphocytes in the pathogenesis of adjuvant arthritis-may point to fruitful areas for investigation of the human reactive arthropathies.